Beta-2 and Beta-3 adrenergic receptors (Beta-2: ADRB2, Beta-3: ADRB3)

Beta-2 and Beta-3 adrenergic receptors are transmembrane G protein-coupled receptors (GPCRs) widely expressed in smooth muscle, adipose, bladder, and various other tissues[1][5][2]. They mediate physiological responses to catecholamines (primarily epinephrine and norepinephrine) by activating intracellular signaling cascades, notably increasing cAMP, which results in smooth muscle relaxation and metabolic regulation[1][2]. Beta-2 adrenergic receptors are key pharmacological targets for bronchodilation in asthma and COPD, while Beta-3 adrenergic receptors are the primary focus for treatment of overactive bladder and are under investigation for metabolic disorders such as obesity and diabetes[6][8][2]. Both receptors are implicated in multiple therapies, and drugs targeting these receptors must balance selectivity, therapeutic efficacy, and safety[5][6][2]. Their molecular structure comprises seven transmembrane domains with characteristic ligand-binding pockets and G protein interaction sites[1][7].

Other names

β2-adrenergic receptorBeta-2 adrenoceptorADRB2β3-adrenergic receptorBeta-3 adrenoceptorADRB3

Agonists activate the receptor, increasing intracellular cAMP via Gs protein coupling, leading to smooth muscle relaxation (e.g., airways for Beta-2, bladder for Beta-3). Antagonists (e.g., some nonselective beta-blockers for Beta-2) block adrenergic signaling. Downstream signaling can also include modulation of metabolic and cardiac processes.